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The gene encoding K-Ras protein is mutated in 20-50% of cases of colorectal cancer (incidence of mutations in K-ras gene in colon cancer cells in various research centers are shown in Table 1).
Huang, "Co-mutation of p53, K-ras genes and accumulation of p53 protein and its correlation to clinicopathological features in rectal cancer," World Journal of Gastroenterology, vol.
Mutational analysis in the present study, however, showed that up to 32 % of patients had mutations in K-ras gene either involving codon 12 or 13.
Analysis of K-ras gene mutations in lung carcinomas: correlation with gender, histological subtypes, and clinical outcome.
Frecuency and Spectrum of Mutation at Codon 12 and 13 of the K-ras Gene in Human Tumors.
The researchers said that the 'Seven-In-Absentia-Homolog' (SIAH) protein seems to be work as a check and balance mechanism in the K-RAS gene, which is known to underlie the abnormal cell growth of pancreatic cancer.
It will soon become standard practice to test all colorectal tumours for mutations in the k-ras gene before treating patients with cetuximab and panitumumab.
Given that somatic mutations of the K-ras gene are observed in ~40% of colorectal cancers (CRCs) (1-3) and in >80% of pancreatic cancers (4), mutant K-ras in stool specimens has been proposed as a potential component of marker combinations aimed at the early detection of these cancers (5-10).
6) Drawbacks in assaying for the k-ras gene mutation include its expression by fewer than half of large adenomas and cancers and its expression by non-neoplastic sources.
A mutation at codons 12 or 13 of the K-ras gene was found in 44 of 115 tumors (38%) tested; p16 methylation was found in 42 tumors (37%).
In the detection of brush cytology specimens, gene mutation exists only if one gene mutate among K-ras gene exon 1 and P53 exon 5, 6, 7, 8.
While conducting a study, researchers from Dana-Farber Cancer Institute (DFCI), Massachusetts General Hospital (MGH) Cancer Center, and Beth Israel Deaconess Medical Center (BIDMC) Cancer Center found that combining two different kinase inhibitors - drugs that interfere with specific cell-growth pathways - led to significant tumour shrinkage in mice with lung cancer driven by mutations in the K-Ras gene.
Some retrospective studies demonstrated that mutation in the K-ras gene is associated with resistance to cetuximab therapy and therefore K-ras mutation is a candidate marker for predicting survival in patients treated with cetuximab.